Mechanisms of Jiangtang No. 3 Prescription in Alleviating Adipose Tissue Insulin Resistance in Diabetic Rats via TLR4/NF-κB/NLRP3 Signaling Pathway-mediated Inflammation
10.13422/j.cnki.syfjx.20252005
- VernacularTitle:基于TLR4/NF-κB/NLRP3信号通路介导的炎症探究降糖3号方改善糖尿病大鼠脂肪组织胰岛素抵抗的机制
- Author:
Tongxun WANG
1
;
Lantian LIU
2
;
Runqi LI
2
;
Haoxiang LI
2
;
Yi ZHAO
2
;
Tian TIAN
2
;
Rufeng MA
3
;
Sihua GAO
2
;
Dandan ZHAO
2
Author Information
1. Qi-Huang Chinese Medicine School， Beijing University of Chinese Medicine， Beijing 100029，China
2. School of Traditional Chinese Medicine， Beijing University of Chinese Medicine， Beijing 100029，China
3. College of Rehabilitation Engineering， China Civil Affairs University， Beijing 102600，China
- Publication Type:Journal Article
- Keywords:
Jiangtang No. 3 prescription;
diabetes;
Toll-like receptor 4/nuclear factor-κB/NOD-like receptor-containing protein 3 （TLR4/NF-κB/NLRP3） signaling pathway;
inflammatory response;
mechanism of action
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(4):109-117
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo observe the effects of Jiangtang No. 3 prescription on inflammatory pathways and insulin resistance-related indicators in rats with type 2 diabetes mellitus （T2DM）， and to elucidate its molecular mechanism in combating diabetes. MethodsA T2DM rat model was established using a high-fat diet combined with intraperitoneal injection of streptozotocin （STZ）. Successfully modeled rats were randomly assigned to the model group， metformin group， and low-， medium-， and high-dose Jiangtang No. 3 prescription groups， and a normal group was also set. Daily gavage was administered for 8 weeks as follows： metformin at 0.1 g·kg-1·d-1， Jiangtang No. 3 prescription granules at 1.62， 3.24， 6.48 g·kg-1·d-1 for the respective dose groups， and sterile water for the normal and model groups. Rat body weight， fasting blood glucose （FBG）， oral glucose tolerance test （OGTT）， and insulin tolerance test （ITT） were measured. After drug intervention， enzyme-linked immunosorbent assay （ELISA） was used to determine serum levels of total cholesterol （TC）， triglycerides （TG）， low-density lipoprotein cholesterol （LDL）， high-density lipoprotein cholesterol （HDL）， non-esterified fatty acids （NEFA）， interleukin （IL）-1β， IL-18， and insulin （INS）. Hematoxylin-eosin （HE） staining was used to observe morphological changes in adipose tissue. Real-time quantitative PCR was used to detect the mRNA expression of Toll-like receptor 4 （TLR4）， nuclear factor-κB （NF-κB）， NOD-like receptor protein 3 （NLRP3）， Caspase-1， IL-1β， IL-18， and gasdermin D （GSDMD） in adipose tissue. Western blot was used to measure the corresponding protein expression levels. ResultsCompared with the model group， Jiangtang No. 3 prescription groups exhibited significantly increased body weight （P<0.05， P<0.01）， significantly reduced FBG （P<0.05， P<0.01）， significant reductions in TC， TG， NEFA， and LDL （P<0.05， P<0.01）， and a significant increase in HDL （P<0.01）. Serum levels of inflammatory mediators IL-1β and IL-18 were significantly decreased （P<0.01）， the homeostatic model assessment of insulin resistance （HOMA-IR） index was significantly reduced （P<0.05， P<0.01）， and adipose tissue pathology was improved. The protein expression levels of TLR4， NF-κB， NLRP3， Caspase-1， IL-1β， IL-18， and GSDMD were markedly decreased （P<0.05， P<0.01）， and the mRNA expression levels of these indicators were also significantly downregulated （P<0.05， P<0.01）. Some effects were superior to those of the positive control drug metformin， and certain indicators exhibited dose-dependent improvements. ConclusionT2DM rats display significant inflammatory responses， disordered glucose and lipid metabolism， and insulin resistance. Jiangtang No. 3 prescription effectively suppresses inflammatory mediators， improves glucose and lipid metabolism and insulin resistance， and ameliorates pathological changes in adipose tissue. Its mechanism may be related to the regulation of the TLR4/NF-κB/NLRP3 signaling pathway in visceral adipose tissue， thereby influencing downstream inflammatory mediators.
